502 CHAPTER 33 Cardiovascular Emergencies
intracranial injury, valvular heart disease, dysrhythmias,
cardiomyopathy, hyperthyroidism, fever, and adult respi-
ratory distress syndrome.6 HF may also occur with oxygen
toxicity syndrome, pneumothorax, uremic pneumonia, in-
tracranial tumors, and drugs such as methotrexate
(Rheumatrex), busulfan (Myleran), and nitrofurantoin
(Furadantin).
HF is characterized by severe dyspnea, orthopnea, fa-
tigue, weakness, abdominal discomfort (secondary to ascites
or hepatic engorgement), dependent edema, distended neck
veins, bilateral rales, third heart sound (gallop), laterally
displaced apical pulse, and hepatomegaly. Assess patient
and ensure adequate airway, breathing, and circulation
(ABCs), then check vital signs, monitor ECG rhythm and
oxygenation, auscultate lungs and heart, and observe for dis-
tended neck veins and peripheral edema.
Therapeutic interventions include maintaining the patient
on bed rest in high-Fowler’s position; administering oxygen,
digitalis, and diuretics; maintaining an IV line at keep-open
rate or use of a saline or intermittent needle therapy; moni-
toring intake and output; and weighing the patient daily. Ad-
ditional therapy may include vasodilators to dilate arteries,
ACE inhibitors to decrease systemic vascular resistance, and
digitalis or other pharmacologic agents (e.g., dobutamine
[Dobutrex]) to increase cardiac output. 9,21 Left ventricular
assistive devices are also used in these patients as a tempo-
rary measure.
Acute Pericarditis
Acute pericarditis is inflammation of the pericardial sac caused
by AMI, trauma, infection, or neoplasms. Among younger pa-
tients, infectious processes such as coxsackie virus, strepto-
cocci, staphylococci, tuberculosis, and Haemophilus influen-
zae can cause pericarditis. Early pericardial friction rub may
occur with pericarditis in conjunction with AMI. Friction rub
occurs when an inflamed area over a transmural infarction
causes the pericardial surface to lose lubricating fluid. Peri-
carditis is most evident 2 to 3 days after an AMI.
Patients with pericarditis have severe chest pain that in-
creases during inspiration and increased activity, fever,
chills, and dyspnea. Tachycardia or other dysrhythmias may
also be present. Pericardial friction rub increases in intensity
when the patient leans forward. The patient has general
malaise with ST segment elevation 1 to 3 mm in all ECG
leads except aVR and V1. Therapeutic intervention includes
oxygen by nasal cannula 4 to 6 L/min, sedation, analgesia,
and bed rest. Antiinflammatory agents and steroids may also
be indicated.6,9,21
Aortic Aneurysm
An aneurysm is “irreversible dilatation of an artery sec-
ondary to a localized weakness of the arterial wall that
may predispose the artery to thrombosis, distal emboliza-
tion, or rupture.” Aneurysms can occur anywhere along
the aorta; however, 80% occur in the abdominal aorta
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
rather than the thoracic aorta. Abdominal aortic
aneurysms (AAA) are more common in individuals ages
50 to 70 years, and account for 10,000 deaths per year.15
One postmortem study suggested 5% of men ages 65 to 74
years had AAA.
The primary etiology of aortic aneurysms is atheroscle-
rosis and related factors; that is, hyperlipidemia, smoking,
diabetes, and hereditary factors. Other causes include arteri-
tis, congenital abnormalities, trauma, infection, and syphilis.
The atherosclerotic process contributes to weakening and
eventual destruction of the medial wall of the artery. Over
time hemodynamic forces of blood flow cause thickening of
the wall and replacement of muscle fibers with fibrous tissue
and calcium deposits. The aneurysm enlarges over time and
the wall tension of the aneurysm increases. Dilation of the
aneurysm allows development of a thrombus, which may be
dislodged and cause thromboembolism distally in the pa-
tient’s circulation, for example, lower extremities.9,21
Three types of aneurysms are fusiform, saccular, and
dissecting. Fusiform aneurysms are characterized by a
segment of artery dilated around the entire circumference
of the artery, whereas a saccular aneurysm dilates only a
portion of the artery. A dissecting aneurysm actually re-
sults in a tear of the artery’s intimal layer, which allows
blood to flow between the intimal and medial layers (Fig-
ure 33-21). Dissecting aneurysms are further classified by
the extent of the tear and location. Type 1 dissection oc-
curs in the ascending aorta and extends beyond the aortic
arch. Type 2 dissection occurs only in the ascending aorta.
Type 3 dissection begins distal to the left subclavian
artery.6
As the aorta dissects, major vessels that branch off the
aorta may be occluded. Occluded vessels include myocar-
dial, cerebral, mesenteric, and renal vessels. Rupture of the
dissection can cause pericardial tamponade or hemorrhage
into the thoracic cavity, resulting in exsanguination, shock,
and imminent death.
Patient Assessment
Fifty percent of patients with aortic aneurysms are asympto-
matic. AAA may be discovered on physical examination
suggested by widened midline pulsation proximal to the
umbilicus. Patients who present to the ED with a leaking or
rupturing AAA have a classic presentation characterized by
extreme back pain accompanied by abdominal pain and ten-
derness with palpation. Back pain may radiate to legs, groin,
or lower back secondary to stretching of the anterior spinal
ligament. Patients with a thoracic aneurysm may complain
of excruciating substernal chest pain felt through to the pos-
terior cavity. Rupture of the aneurysm compromises hemo-
dynamic stability and blood flow distal to the aneurysm.
Signs and symptoms include dyspnea, orthopnea, diaphore-
sis, pallor, apprehension, syncope, tachycardia, unilateral
absence of major pulses, bilateral blood pressure differ-
ences, hypertension, pulsation at the sternoclavicular joint,
murmur of aortic insufficiency (in ascending aortic
aneurysm), hemiplegia or paraplegia, and shock.

FIGURE 33-21 Dissecting aortic aneurysm.
Patient Management
The most common diagnostic test for aortic aneurysm is the
chest radiograph. Patients must be in an upright position to
validate the widened mediastinum. Extremely large
aneurysms may appear as soft masses, displace other or-
gans, or cause abnormal gas patterns. Other diagnostic tests
that may be used if the patient is hemodynamically stable in-
clude ultrasound and computed tomography scan.
Therapeutic intervention includes placing the patient in a
high-Fowler’s position, administering high-flow oxygen,
and inserting two large-bore IV catheters with lactated
Ringer’s solution. Maintaining blood pressure control is
critical. If hypertension is present such drugs as nitroprus-
side sodium (Nipride) are used to decrease blood pressure.
If the patient has hypovolemic shock, intervention focuses
on maintaining ABCs, fluid resuscitation, and preparing for
emergency surgery.
Hypertensive Crisis
Hypertension can be defined as a systolic blood pressure
140 mm Hg and/or a diastolic pressure 90 mm Hg.
When blood pressure becomes abruptly elevated to extreme
levels, the patient has a life-threatening situation. An esti-
mated 50 million people in the United States have hyperten-
sion. The actual incidence of hypertensive crisis is relatively
rare, occurring in approximately 1% of the hypertensive
population.24
Hypertensive crisis is categorized by the degree of acute-
target end-organ damage and the rapidity with which the
blood pressure must be lowered. Hypertensive crisis has
been further categorized into hypertensive emergencies and
hypertensive urgencies. Hypertensive emergencies are those
clinical situations in which excessively high blood pressure
must be lowered quickly, within minutes to hours, to prevent
new or worsening organ damage. Hypertensive urgencies
develop over days to weeks and generally demonstrate an el-
evated diastolic blood pressure without signs of end organ
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
CHAPTER 33 Cardiovascular Emergencies 503
damage. Determination of end-organ damage is made by
clinical presentation.
Regardless of underlying mechanism of hypertension, el-
evated blood pressure increases systemic or peripheral vas-
cular resistance and cardiac output. These increases perpet-
uate the cycle by stimulating release of catecholamines,
which increases a sympathetic activity and activates the renin-
angiotensin system. The net result is continued increases in
blood pressure. Hypertensive crisis usually occurs in pa-
tients with a history of hypertension. Other conditions that
may cause or precipitate hypertensive crisis include renal
parenchymal disease (e.g., acute glomerulonephitis, vasculi-
tis), endocrine problems (e.g., pheochromocytoma, Cush-
ing’s syndrome), use of sympathomimetic drugs (cocaine,
amphetamines, phencyclidine, lysergic acid diethylamide,
diet pills) and food-drug interactions (e.g., monoamine oxi-
dase and tyramine interaction).37
Patient Assessment
Patients with hypertensive crisis usually have DBP higher
than 120 mm Hg. Primary symptoms are consistent with
new or evolving end-organ damage. Increase in systemic
peripheral vascular resistance and sympathetic stimulation
imposed by the significant hypertension increase myocar-
dial workload and myocardial oxygen consumption.
Symptoms associated with cardiovascular manifestations
include congestive heart failure, chest pain, angina, and
AMI. Neurologic changes include headache, nausea, vom-
iting, dizziness, visual disturbances (e.g., blurred vision,
temporary visual loss, decreased visual acuity, photopho-
bia), altered mental states (e.g., agitation, confusion,
lethargy, coma), and seizures.6 Other neurologic symptoms
include focal cranial nerve palsy, sensory deficits, motor
deficits, aphasia, and hemiparesis. Fundoscopic evaluation
may reveal papilledema from effects of hypertension on
retina7.
Patient Management
In addition to cardiac and vital sign monitoring, IV access
should be established. An arterial line provides the most ac-
curate blood pressure readings; however, a noninvasive
blood pressure device can also be used for continuous BP
monitoring. The goal of management is to lower SBP to 100
to 110 mm Hg. Intravenous pharmacologic agents such as
nitroprusside sodium (Nipride), nitroglycerin (Tridil),
fenoldopam mesylate (Corlopam), enalaprilat (Vasotec), la-
betalol hydrochloride (Normodyne), nicardipine hydrochlo-
ride (Cardene), esmolol hydrochloride (Brevibloc), phento-
lamine mesylate (Regitine), and propranolol (Inderal) are
used so they can be titrated for safe, effective reduction of
SBP. Assess the patient’s response to these agents (i.e., pre-
senting symptoms improved or new symptoms not present).
SUMMARY
Cardiovascular attacks are frequent and challenging aspects
of emergency nursing. Box 33-4 lists a few nursing diagnoses